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兴奋剂与肺动脉高压:最新进展

Stimulants and Pulmonary Arterial Hypertension: An Update.

作者信息

Ramirez Ramon L, De Jesus Perez Vinicio, Zamanian Roham T

机构信息

Department of Medicine, Stanford University School of Medicine, Stanford, CA.

Division of Pulmonary and Critical Care Medicine, Stanford University School of Medicine, Vera Moulton Wall Center for Pulmonary Vascular Disease, Stanford, CA.

出版信息

Adv Pulm Hypertens. 2018;17(2):49-54. doi: 10.21693/1933-088X-17.2.49.

DOI:10.21693/1933-088X-17.2.49
PMID:31656550
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6815676/
Abstract

The connection between stimulants and pulmonary arterial hypertension (PAH) was first made apparent in the 1960s during an outbreak associated with anorexigen (amphetamine-like appetite suppressants) use. Since then, a total of 16 drugs and toxins have been linked to PAH (ie, drug and toxin-associated PAH [DT-APAH]), including illicit stimulants like methamphetamine. Recently, basic science research and novel genomic studies have started to shed light on possible pathologic and genetic mechanisms implicated in disease development, namely loss of function variants in genes involved in drug detoxification. This review will discuss the history and current state of knowledge regarding stimulants and their association with PAH. It will also discuss clinical management of patients with DT-APAH. Lastly, it will highlight the importance of ongoing research efforts to identify susceptibility factors implicated in DT-APAH and the need for increased pharmacovigilance and awareness to identify new drugs that may be risk factors for PAH. Ultimately, this may be our best strategy to improve clinical outcomes and prevent deadly future outbreaks of DT-APAH.

摘要

兴奋剂与肺动脉高压(PAH)之间的联系最早在20世纪60年代与使用食欲抑制剂(类似苯丙胺的食欲抑制剂)相关的一次暴发中显现出来。从那时起,共有16种药物和毒素与PAH有关(即药物和毒素相关的PAH [DT-APAH]),包括甲基苯丙胺等非法兴奋剂。最近,基础科学研究和新的基因组研究开始揭示疾病发展中可能涉及的病理和遗传机制,即参与药物解毒的基因功能丧失变异。本综述将讨论兴奋剂及其与PAH关联的历史和当前知识状态。它还将讨论DT-APAH患者的临床管理。最后,它将强调正在进行的研究工作对于识别DT-APAH中涉及的易感因素的重要性,以及提高药物警戒和认识以识别可能是PAH风险因素的新药的必要性。最终,这可能是我们改善临床结果并预防未来DT-APAH致命暴发的最佳策略。

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Mazindol: a risk factor for pulmonary arterial hypertension?
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Am J Physiol Lung Cell Mol Physiol. 2017 Aug 1;313(2):L252-L266. doi: 10.1152/ajplung.00453.2016. Epub 2017 May 4.
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Serotonin transporter is not required for the development of severe pulmonary hypertension in the Sugen hypoxia rat model.在Sugen低氧大鼠模型中,严重肺动脉高压的发展不需要血清素转运体。
Am J Physiol Lung Cell Mol Physiol. 2015 Nov 15;309(10):L1164-73. doi: 10.1152/ajplung.00127.2015. Epub 2015 Sep 18.
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